Osteoporosis resident survival guide

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Osteoporosis Resident Survival Guide Microchapters


Osteoporosis was first discovered by John Hunter, British surgeon, in 1800's. Osteoporosis may be classified as primary or secondary, based on etiology; while, it is divided in to osteopenia, osteoporosis, and severe osteoporosis, based on disease severity. Osteoporosis occurs as result of an imbalance between bone resorption and bone formation. Major contributing factors to the development of osteoporosis include estrogen deficiency and aging. These factors might lead to osteoporosis by reactive oxygen species (ROS) mediated damage to osteocytes. Decrease in the capability of autophagy in osteocytes is another important factor which makes them vulnerable to oxidative stress. Genes involved in the pathogenesis of osteoporosis can be categorized in four main groups which include the osteoblast regulatory genes, osteoclast regulatory genes, bone matrix elements genes, and hormone/receptor genes. Osteoporosis must be differentiated from other diseases associated with a decrease in bone mineral density (BMD) such as idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis. Osteoporosis is a major health problem involving 43.9% (43.4 million) of male and female population in the United States. Risk of osteoporosis increases with age. Osteoporosis usually involves individuals of age 80 years and older. White females and African-American males have the highest incidence among other races. Risk factors for osteoporosis are of two types, non-modifiable and modifiable factors. Non-modifiable risk factors include age, sex, menopause, and family history. Modifiable risk factors include smoking, alcohol consumption, immobility, glucocorticoid abuse, and use of proton pump inhibitor (PPI). Risk of fracture due to osteoporosis threatens every second postmenopausal women and every fifth old man. The 10-year risk for any osteoporosis-related fracture in 65-year-old white woman with no other risk factor is 9.3%. According to USPSTF guidelines, all women ≥ 65 years along with women < 65 years old with high risk of fracture must be screened for osteoporosis. There is no recommendation to screen men for osteoporosis. Screening for osteoporosis can be done by dual energy x-ray absorptiometry (DXA) of both hips and lumbar spine, and quantitative ultrasonography of the calcaneus. If left untreated, most of the patients with osteoporosis may develop fractures. With appropriate and timely usage of medications along with calcium and/or vitamin D supplementation, the outcome of osteoporosis is usually good. Apart from risk of death and other complications, osteoporotic fractures are associated with a decreased quality of life secondary to immobility and emotional disturbances. The impact of osteoporosis and osteoporotic fractures on human life becomes intense with aging. There are various lifestyle modifications that can prevent the development of osteoporosis, these include calcium and vitamin D supplementation, diet, exercise, smoking cessation, minimizing alcohol consumption, and fall prevention. The mainstay of treatment in primary osteoporosis is lifestyle modifications. High risk patients and patients with past history of osteoporotic fracture, require medical therapy. Bisphosphonates are the first line treatment for osteoporosis. Raloxifene is the second line treatment for osteoporosis in postmenopausal women and is also used for prevention. Denosumab is a human monoclonal antibody designed to inhibit RANKL (RANK ligand), a protein that acts as the primary signal for bone removal. Denosumab is used to treat osteoporosis in elder men and postmenopausal women. Teriparatide and abaloparatide are human recombinant parathyroid hormones used to treat postmenopausal woman with osteoporosis at high risk of fracture or to increase bone mass in men with osteoporosis.


Osteoporosis may be classified into several subtypes based on disease origin, and disease severity. Osteoporosis may be classified into several subtypes based on disease origin, and disease severity.

Osteoporosis classifications
Based on
Based on
Children and Adolescents
Children, Adolescents, and Adults
Z-score measurement
T-score measurement
Bone loss due to other diseases?
Z-score > -2.0
without fracture history
Z-score < -2.0 and significant fracture history
(2 or more long bone fractures before 10 years of age
3 or more long bone fractures before 19 years of age)
One or more vertebral fractures occurring in the absence of local disease or high-energy trauma
-1 > T-score > -2.5
T-score ≤ -2.5
T-score ≤ -2.5
history of fracture
Severe osteoporosis
Primary osteoporosis
Secondary osteoporosis

Juvenile Osteoporosis (JO)

Osteoporosis in children and adolescents is rare, usually is due to some comorbidities or medications, secondary osteoporosis. Surprisingly, no significant causes have been found for rare cases, idiopathic osteoporosis.

No matter what causes it, juvenile osteoporosis can be a significant problem because it occurs during the child’s prime bone-building years. From birth through young adulthood, children steadily accumulate bone mass, which peaks sometime before age 30. The greater their peak bone mass, the lower their risk for osteoporosis later in life. After people reach their mid thirties, bone mass typically begins to decline—very slowly at first but increasing in their fifties and sixties. Both heredity and lifestyle choices—especially the amount of calcium in the diet and the level of physical activity influence the development of peak bone mass and the rate at which bone is lost later in life.

Secondary Osteoporosis

As the primary condition, juvenile idiopathic arthritis (also known as juvenile rheumatoid arthritis) provides a good illustration of the possible causes of secondary osteoporosis. In some cases, the disease process itself can cause osteoporosis. In other cases, medication used to treat the primary disorder may reduce bone mass. For example, drugs such as prednisone, used to treat severe cases of juvenile idiopathic arthritis, negatively affect bone mass. Finally, some behaviors associated with the primary disorder may lead to bone loss or reduction in bone formation. For example, a child with juvenile idiopathic arthritis may avoid physical activity, which is necessary for building and maintaining bone mass, because it may aggravate his or her condition or cause pain.[1]

Idiopathic Juvenile Osteoporosis

Idiopathic juvenile osteoporosis (IJO) is a primary condition with no known cause. It is diagnosed after other causes of juvenile osteoporosis have been excluded. This rare form of osteoporosis typically occurs just before the onset of puberty in previously healthy children. The average age at onset is 7 years, with a range of 1 to 13 years. Most children experience complete recovery of bone.


Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of osteoporosis, however complications resulting from untreated osteoporosis are common.

Common and Less Common Causes

Musculoskeletal genetic disorder
Progeria genetic disorder
Hormonal disorder
Medical condition
•Excessive Dieting
Alpha thalassemia
Diamond-Blackfan anemia
Fabry's disease
Glycerol kinase deficiency
Lobstein disease
Menkes Disease[3]
Osteogenesis imperfecta
Mixed connective tissue disease
Paget's disease of bone
Prader-Willi syndrome
Prolidase deficiency
•Thick skull syndrome
•Systemic infantile hyalinosis
Waldenstrom's macroglobulinemia
Ehlers-Danlos syndrome- progeroid form
Geroderma osteodysplastica[4]
Hutchinson Gilford Syndrome[5]
Hyperglycerolemia - infantile form
Infantile sialic acid storage disorder
Premature aging
•Pseudoprogeria syndrome
Storm syndrome
Werner syndrome
Calcium deficiency
Copper deficiency[6]
Female athlete triad
Protein deficiency
•White Phosphorus poisoning
Zero gravity
Gonadal dysgenesis
Primary hypoparathyroidism
Adrenal adenoma
Adrenal incidentaloma
Adrenocortical carcinoma
Aromatase deficiency
Cushing's syndrome[7]
Functioning pancreatic endocrine tumor
Hashimoto's Thyroiditis
Kallmann syndrome
Klinefelter syndrome[8]
Lactotroph adenoma
Oophorectomy - bilateral
Sub clinical hypothyroidism
Turner's syndrome
Fluticasone (aerosol)
Chronic renal failure
Ankylosing spondylitis
Chronic Hepatitis
Chronic obstructive pulmonary disease
Cystic fibrosis
Hyper IgE syndrome / Job syndrome
Primary biliary cirrhosis
Sickle cell anemia[13]
Wilson's Disease

FIRE: Focused Initial Rapid Evaluation

Osteoporosis; prevention, diagnosis, and management[14][15][16][17][18]

Lifestyle modifications
Calcium Supplementation
Vitamin D supplementation
Smoking cessation
Reduced alcohol consumption
Hip protectors
Fall protection
• Balance, strength and functional training exercises
• 9-18 yrs: 1,300 mg
• 19-50 yrs: 1,000 mg
• 51-70 yrs: 1,200 mg
• 71 and more yrs: 1,200 mg
• 50-70 yrs: 1,000 mg
• 71 and more yrs: 1,200 mg
• 9-18 yrs: 600 IU
• 19-50 yrs: 600 IU
• 51-70 yrs: 600 IU
• 71 and more yrs: 800 IU
• More than 50 yrs: 800-1,000 IU

Serum vitamin D level of 20 ng per mL (50 nmol per L) is recommended for good bone health
• Stop-smoking program and nicotine patch
Limit to:
• One drink/day for women
• Two drinks/day for men

Moderate alcohol may associated with slightly higher BMD and lower fracture risk in postmenopausal women
• Hard and soft hip protectors, upon preference
Multifactorial interventions:
• Individual risk assessment
Tai Chi Chuan and other exercise programs
• Home safety assessment and modification by an occupational therapist
• Gradual withdrawal of psychotropic medication
Visual impairment correction
• Improve mobility
Chronic glucocorticoid (GC) use
Children and adolescent
< 40 yrs
≥ 40 yrs
Clinical fracture risk assessment:
• Within 6 months of the start of GC treatment
• Every 12 months during GC treatment
No need to bone mineral density measurement
As soon as possible but at least within 6 months of the initiation of GC treatment if:
• High fracture risk
• Significant osteoporotic risk factors (malnutrition, significant weight loss or low body weight, hypogonadism, secondary hyperparathyroidism, thyroid disease, family history of hip fracture, smoking, alcohol use)

Every 2-3 yrs of GC treatment if:
• Moderate-to-high fracture risk
•• History of previous fracture
•• BMD Z score < -3
•• Received very high-dose prednisone [≥30 mg/day and cumulative dose >5 gm]
•• Risks for poor medication adherence or absorption
•• Multiple osteoporotic risk factors
As soon as possible but at least within 6 months of the initiation of GC treatment:
• FRAX with glucocorticoid dose correction

Every 1-3 yrs of GC treatment if:
• Continued GC treatment and are not treated with an osteoporosis medication beyond calcium and vitamin D
• Receiving very high doses of GCs (initial prednisone dose ≥30 mg/day, cumulative dose > 5 gm in the previous year)
• Positive history of osteoporotic fracture

Every 2-3 yrs of GC treatment if:
• Continued GC treatment and are currently treated with an osteoporosis medication in addition to calcium and vitamin D
• Receiving very high doses of GCs (initial prednisone dose ≥ 30 mg/day, cumulative dose > 5 gm in the previous year)
• Positive history of osteoporotic fracture occurring after ≥ 18 months of treatment with antifracture medication (other than calcium and vitamin D)
• Risks for poor medication adherence or absorption
• Other significant osteoporotic risk factors
• 18 yrs of age or 2 yrs after chemotherapy
• Severe diseases
• Low body weight
• Chronic corticosteroid use
• Delayed puberty
Gonadal failure
• History of low-impact fracture
• Young Hypogonadal
• More than 70 yrs
• Less than 70 yrs with:
••Low body weight
••Prior fracture
••High risk medication use
••Disease or condition associated with bone loss
• More than 65 yrs
Postmenopausal women younger than 65 yrs with:
••History of fragility fracture
•• Weigh less than 127 lb (58 kg)
••Medications or diseases that cause bone loss
•• Parental history of hip fracture
•• smoking
•• Alcoholism
•• Rheumatoid arthritis.
Dual energy X-ray absorptiometry (DEXA)
Under glucocorticoid therapy
No glucocorticoid therapy
Calcium and vitamin D and life style modification
Low risk
Moderate/High risk
No further treatment

Monitor with yearly fracture risk assessment
with BMD testing every 2-3 years
depending on risk factors
Age < 40 years

1. History of osteoporotic fracture, OR
2. Z score < -3 at hip or spine and
prednisolone ≥ 7.5 mg/d, OR
3. >10%/year loss of BMD at hip or spine and
prednisolone ≥ 7.5 mg/d, OR
4. Very high dose glucocorticoid and > 10 years
Age ≥ 40 years

1. History of osteoporotic fracture, OR
2. Men > 50 years and postmenopausal women
with a BMD T-score ≤ -2.5, OR
3. FRAX 10-year risk for major osteoporotic fracture > 10%, OR
4. FRAX 10-year risk for hip osteoporotic fracture > 1%, OR
5. Very high dose of glucocorticoid
BMD T-score is not used for children until 20 yrs of age

Osteoporosis defined as:
• One or more vertebral fractures occurring in the absence of local disease or high-energy trauma
• low bone density (BMD Z-scores < –2.0) and a significant fracture history
(2 or more long bone fractures before 10 years of age
3 or more long bone fractures before 19 years of age)
-2.5 < BMD < -1
10-year risk of major osteoporotic fracture of at least 20% or a risk of hip fracture of at least 3%
• Treat with an oral bisphosphonate

• Second-line therapy: teriparatide

• Other suggested therapies (in order of preference)
for high risk woman for whom the previous drugs are not appropriate:

IV bisphosphonate
• Treat with an oral bisphosphonate
• Other suggested therapies (in order of preference):

IV bisphosphonate
Raloxifene for postmenopausal women if no other therapy is available
Calcium daily intake:
• 500 mg for children 1 to 3 years of age
• 800 mg for children 4 to 8 years of age
• 1300 mg for children and adolescents 9 to 18 years of age
Weight-bearing activity and Short periods of high-intensity exercise
• Jumping 10 minutes/day, 3 times/week
Inflammatory bowel disease (IBD)
• Anti tumor necrosis factor alpha (TNF-α)
Moderate to severe osteogenesis imperfecta (2 or more fractures in a year or vertebral compression fractures)
• Treat with an oral bisphosphonate

• If patient has GI problem
IV bisphosphonate
Zoledronic acid

• If patient not tolerate bisphosphonate
Pharmacotherapy efficacy
Intervention Spine BMDHip BMDVertebral fractureNon-vertebral fracture
AlendronateHighly effectiveHighly effectiveModerately effectiveNot adequately evaluated
EtidronateHighly effectiveHighly effectiveHighly effectiveNot adequately evaluated
RisedronateHighly effectiveHighly effectiveHighly effectiveNot adequately evaluated
Zoledronic acidHighly effectiveHighly effectiveNot adequately evaluatedNot adequately evaluated
TeriparatideHighly effectiveHighly effectiveHighly effectiveNot adequately evaluated
Pharmacotherapy efficacy
Vertebral fractureNon-vertebral fractureHip fracture
AlendronateHighly effectiveHighly effectiveHighly effective
Etidronate Highly effectiveModerately effectiveNot adequately evaluated
Ibandronate Highly effectiveHighly effectiveNot adequately evaluated
Risedronate Highly effectiveHighly effectiveHighly effective
Zoledronic acidHighly effectiveHighly effectiveHighly effective
Denosumab Highly effectiveHighly effectiveHighly effective
Calcitriol Highly effectiveModerately effectiveNot adequately evaluated
Raloxifene Highly effectiveNot adequately evaluatedNot adequately evaluated
Strontium ranelateHighly effectiveHighly effectiveHighly effective
Teriparatide Highly effectiveHighly effectiveNot adequately evaluated
Recombinant human PTH (1-84)Highly effectiveNot adequately evaluatedNot adequately evaluated
Hormone replacement therapy (HRT)Highly effectiveHighly effectiveHighly effective



Lifestyle modifications

Intervention Effect on outcomes[16]
Bone mineral density (BMD) Spine fracture Hip fracture
Exercise Highly effective Moderately effective Moderately effective
Calciumvitamin D) supplements Highly effective Moderately effective Moderately effective
Dietary calcium Moderately effective Moderately effective Moderately effective
Smoking cessation Moderately effective Moderately effective Moderately effective
Reduced alcohol consumption Mildly effective Mildly effective Moderately effective
Fall prevention programmes - Mildly effective Mildly effective
Hip protectors - - Moderately effective


Group[18] Drug (brand) Dosage Route Usage Interval Contraindications
Bisphosphonate Alendronate (Fosamax) 35 mg (7×5 gm) Per oral (PO) Prevention Weekly (7×daily)
70 mg (7×10 mg) PO Treatment Weekly (7×daily)

(Fosamax Plus D)

70 mg plus 2,800 IU

70 mg plus 5,600 IU

PO Treatment Weekly
Risedronate (Atelvia) 35 mg (delayed release) PO Treatment Weekly
Risedronate (Actonel) 35 mg PO Prevention and treatment Weekly
150 mg PO Monthly
Risedronate/calcium carbonate (Actonel with calcium) 35 mg per week (day 1) plus 1,250 mg calcium for no-risedronate days (days 2 through 7 of seven day treatment cycle) PO Prevention and treatment Weekly
Ibandronate (Boniva) 150 mg PO Prevention and treatment Monthly
3 mg IV Treatment Every 3 months
Zoledronic acid (Reclast) 5 mg IV Prevention Every 2 years
5 mg IV Treatment Annually
Selective estrogen receptor modulator (SERM) Raloxifene (Evista) 60 mg PO Prevention and treatment Daily
Human monoclonal anti RANKL antibody Denosumab (Prolia) 60 mg Subcutaneous (SC) Treatment Every 6 months
Human monoclonal anti sclerostin antibody Romosozumab  210 mg SC Treatment Monthly -
Parathormone recombinant Teriparatide (Forteo) 20 mcg SC Treatment Daily (approved for less than 2 years use)
Abaloparatide (Tymlos) 80 mcg SC Treatment Daily (approved for less than 2 years use) -
Hormonal Calcitonin (Miacalcin) 100 units SC Treatment (in women more than five years past menopause) Daily
200 units Intranasal Daily


Lifestyle modification for preventing osteoporosis

To reduce the risk of bone loss and osteoporotic fractures, women with osteoporosis or who are at risk of osteoporosis should be counseled about lifestyle changes, including:

Medications for preventing osteoporosis in postmenopausal women



Follow up

In women older than 65 years with low bone mass, as indicated by bone mineral density reports, the World Health Organization’s Fracture Risk Assessment Tool (FRAX; available at http://www.shef.ac.uk/FRAX/index.aspx) should be used to establish if a woman is at increased risk of fracture.

Among those not at increased risk of fracture, screening should be performed:

  • Every 15 years for women older than 65 years with a normal bone mineral density or a T-score of -1.5 or greater
  • Every five years for women with a T-score of -1.5 to -1.99
  • Every year for women with a T-score of -2.0 to -2.49


  • Don't use T-score for interpreting children BMD score; therapeutic option has to be decided based on Z-score in children, which is matched by age, sex, and race.
  • Avoid certain drugs that can decrease bone mass in high risk patients, as much as possible. These include proton pump inhibitors, corticosteroids, and some of the newer antidepressants.
  • Don't consider any pharmacological therapy indefinite in duration. After the initial treatment period, which depends on the pharmacological agent, a comprehensive risk assessment should be performed.
  • There is no uniform recommendation that applies to all patients and duration decisions need to be individualized.[16]
  • Don't utilize any procedure to measure bone density unless the results will influence the patient’s treatment decision.[22]
  • Don't prescribe more than the safe upper limit for vitamin D intake for the general adult population, 4000 IU/day.[23]
  • Don't prescribe bisphosphonates for patients with esophageal problems or inability to sit or stand upright.


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